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LC-MS/MS analysis of human brain fibroblast-secreted molecules

ABSTRACT: Our study showed that fibroblasts significantly attenuated blood-brain barrier (BBB) disruption in an in vitro intracerebral hemorrhage (ICH) model. Since fibroblasts and brain microvascular endothelial cells were not in direct contact in this model, we reasoned that fibroblasts did so by secreting molecules with BBB-protective function. Here, we further screened fibroblast-secreted molecules in this in vitro ICH model by mass spectrometry.

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Fibroblast

DISEASE(S): Intracerebral Hemorrhage

SUBMITTER: Yao Yao

LAB HEAD: Yao Yao

PROVIDER: PXD037247 | Pride | 2022-11-14

REPOSITORIES: Pride

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			Action	DRS
	F010379.mgf	Mgf
	F010379.mzid.gz	Mzid
	F010380.mgf	Mgf
	F010380.mzid.gz	Mzid
	F010381.mgf	Mgf

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Publications

Fibroblasts repair blood-brain barrier damage and hemorrhagic brain injury via TIMP2.

Xu Lingling L Nirwane Abhijit A Xu Ting T Kang Minkyung M Devasani Karan K Yao Yao Y

Cell reports 20221101 8

The function of fibroblasts in intracerebral hemorrhage (ICH) remains elusive. By targeting Col1α1, a fibroblast-specific marker, we generate mice with ablated Col1α1<sup>+</sup> fibroblasts. These mutants show exacerbated blood-brain barrier (BBB) damage, enlarged injury volume, and worse neurological function, highlighting a beneficial role of Col1α1<sup>+</sup> fibroblasts in ICH. Echoing these findings, fibroblasts significantly decrease endothelial permeability in an in vitro ICH model. Nex ...[more]

PMID: 36417884

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Age-associated changes in murine endothelial gene expression and chromatin accessibility correlate with impaired blood-brain barrier integrity and elevated risk of intracerebral hemorrhage [RRBS]

Project description:Intracerebral hemorrhage (ICH), a devastating form of stroke, is a leading global cause of human death and disability. The major risk factors for ICH include increasing age, hypertension and cerebral amyloid angiopathy. Despite high mortality and morbidity associated with ICH, the mechanisms leading to blood-brain barrier (BBB) dysfunction with age and development of hemorrhagic stroke is poorly understood. In the vasculature of the central nervous system, endothelial cells (ECs) constitute the core component of the BBB and provide a physical barrier due to tight junctions, adherens junctions, and basement membrane layers. In this study, we show in brains of mice that incidents of intracerebral bleeding increase with advancing age. After isolation of an enriched population of cerebral ECs, we studied gene expression in ECs isolated from murine brains of increasing ages of 2, 6, 12, 18, and 24 months. The study reveals age-dependent dysregulation of 1388 genes in the ECs, including many involved in the maintenance of BBB and vascular integrity. Since epigenetic mechanisms regulate gene expression, we also investigated age-dependent changes at the levels of CpG methylation and accessible chromatin in cerebral ECs. Our study reveals correlations between age-dependent changes in chromatin structure and gene expression. We find significant age-dependent downregulation of the apelin receptor (Aplnr) gene along with an age-dependent reduction in chromatin accessibility of the promoter of this gene. Aplnr is known to play a crucial role in positive regulation of vasodilation and is implicated in vascular health. Interestingly, we also observe an age-dependent reduction in the protein expression levels of the apelin receptor in the brain, potentially implicating the apelin receptor to be critical for the increased risk of intracerebral hemorrhage with ageing.

2023-09-20 | GSE218648 | GEO

Age-associated changes in murine endothelial gene expression and chromatin accessibility correlate with impaired blood-brain barrier integrity and elevated risk of intracerebral hemorrhage [ATAC-seq]

2023-09-20 | GSE218647 | GEO

Examining Transcriptomic Alterations in Rat Models of Intracerebral Hemorrhage and Severe Intracerebral Hemorrhage

Project description:Intracerebral hemorrhage (ICH) is a life-threatening condition associated with significant morbidity and mortality. Understanding the molecular mechanisms underlying ICH and its severe form is crucial for developing effective therapeutic strategies. This study investigates transcriptomic alterations in rodent models of ICH and severe intracerebral hemorrhage to shed light on the genetic pathways involved in hemorrhagic brain injury. We performed principal component analysis, revealing distinct principal component segments of normal rats compared to intracerebral hemorrhage and severe intracerebral hemorrhage rats. We further employed heatmaps and volcano plots to identify differentially expressed genes and utilized bar plots and KEGG pathway analysis to elucidate the different molecular pathways involved. Using comprehensive RNA sequencing and bioinformatics analyses, we identified a multitude of differentially expressed genes in both the ICH and severe ICH models. Our results revealed 5679 common genes among the normal, intracerebral hemorrhage, and severe intracerebral hemorrhage groups in the upregulated genes group, and 1196 common genes in the downregulated genes. A volcano plot comparing the groups further highlighted common genes, including PDPN, TIMP1, SERPINE1, TUBB6, and CD44. These findings underscore the complex interplay of genes involved in inflammation, oxidative stress, and neuronal damage. Furthermore, pathway enrichment analysis uncovered key signaling pathways, including the TNF signaling pathway, protein processing in the endoplasmic reticulum, MAPK signaling pathway, and Fc gamma R-mediated phagocytosis, implicated in the pathogenesis of ICH.

2024-06-11 | GSE264394 | GEO

RNA-seq of perihaematomal and anatomically matched contralateral brain tissue after intracerebral hemorrhage

Project description:Secondary injury causes death and dependence after spontaneous intracerebral haemorrhage (ICH). Having found that ICH is associated with activation of genes regulated by the transcription factor NRF2, we performed bulk RNA sequencing of perihaematomal and anatomically matched contralateral brain homogenate obtained at autopsy from a cohort of patients who died either within 24h of ICH or between 4-14 days of ICH onset, to investigate the spatiotemporal evolution of this Nrf2 activation.

2024-08-13 | E-MTAB-14323 | biostudies-arrayexpress

RNA-seq of microglia and monocyte-derived cells in Nrf2 knockout and wild-type mice after induced intracerebral hemorrhage or sham treatment

Project description:Secondary injury causes death and dependence after spontaneous intracerebral haemorrhage (ICH). Having found that ICH is associated with activation of genes regulated by the transcription factor Nrf2, particularly in mononuclear myeloid cells (for example, monocyte-derived cells (MdC) and microglia), we sought to determine the importance of Nrf2 to mononuclear myeloid cell responses and their impact on ICH pathology. We used intrastriatal injection of collagenase to induce ICH in both wild-type mice, and knockout mice with Cx3cr1-Cre-mediated excision of Nrf2 (Nfe2l2) exon 5.

2024-08-13 | E-MTAB-14324 | biostudies-arrayexpress

Genome-wide DNA methylation pattern in whole blood associated with primary intracerebral hemorrhage

Project description:To reveal the role of DNA methylation in peripheral blood from primary intracerebral hemorrhage(ICH) ,DNAs from 30 ICH patients and 34 matched controls were analyzed by methylation microarray. In total, we identified 1377 hypomethylated and 153 hypermethylated differentially methylated positions (DMPs) in peripheral blood from ICH patients compared to healthy controls.

2021-07-10 | GSE179759 | GEO

Transcriptome profiling of rat brain samples in two age groups in responding to intracerebral hemorrhage

Project description:Aging-induced decline of endogenous neuroprotection has been shown to aggravate intracerebral hemorrhage (ICH)-induced acute brain injury, however, the underlying mechanisms in brain are still little known. In this study, we applied a rat ICH model to study the transcriptional responses in the early and late aging (13-month and 22-month old) rats that show substantial differences in brain damage and recovery. Transcriptome analysis (RNA-seq) reveals that brain expression of neuroinflammation genes is similarly and selectively upregulated in ICH, which includes genes in the cellular response to interferon gamma function. We show that the anti-IFN-γ treatment effectively reduces ICH-induced acute brain injury.

2020-04-27 | GSE149317 | GEO

Analysis of Age-Dependent Transcriptomic Changes in Response to Intracerebral Hemorrhage in Mice

Project description:To investigate age-dependent transcriptomic changes between young or aged intracerebral hemorrhage mice, we established collagenase IV-induced intracerebral hemorrhage mice models. Intracerebral hemorrhage was induced by infusion of sterile collagenase IV in ipsilateral caudate putamen of brain. We then performed gene expression profiling analysis using data obtained from RNA-seq of brain perihematomal tissues from young or aged ICH mice 24 hours after intracerebral hemorrhage.

2022-04-29 | GSE200575 | GEO

High-Throughput mRNA Sequencing Reveals Potential Therapeutic Targets of Febuxostat in Secondary Injury After Intracerebral Hemorrhage

Project description:Febuxostat is a urate-lowering medication for the treatment of patients with gout. This study was performed to elucidate the effects and underlying mechanisms of febuxostat on neuronal injury induced by intracerebral hemorrhage (ICH) in mice. The results showed that the administration of febuxostat improved neurological severity scores and blood-brain barrier (BBB) permeability. Moreover, febuxostat attenuated neuronal cell death and cytokine levels compared with the ICH group. Next, we conducted a transcriptome analysis of the neuroprotective effects of febuxostat. The overlapping significant differentially expressed genes (DEGs) were identified. Gene ontology (GO) analysis revealed that the overlapping significant DEGs were most enriched in five items. The intersecting DEGs of the aforementioned five pathways were Wisp1, Wnt7b, Frzb, and Pitx2. In addition, GO terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways revealed that DEGs were mainly involved in the wnt signaling pathway. Furthermore, the expression of Wisp1 and Wnt7b in the perihematomal region at 72 h post-ICH was observed. The results showed that both Wisp1 and Wnt7b were increased in the ICH group and were decreased by the administration of febuxostat. Taken together, the study showed that febuxostat protected against secondary brain injury after ICH and the Wnt7b-Wisp1 pathway was closely related to neuroprotective effects.

2022-06-09 | GSE193076 | GEO

Expression data from human brain samples

Project description:Spontaneous intracerebral hemorrhage (ICH) represents about 15% of all strokes and is associated with high mortality rates. Our aim was to identify the gene expression changes and biological pathways altered in the brain following ICH. Twelve brain samples were obtained from four deceased patients who suffered an ICH including perihematomal tissue (PH) and the corresponding contralateral white (CW) and grey (CG) matter.

2010-09-24 | GSE24265 | GEO

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